Case report and literature review on concurrent t-AML and LNTB treated with chemoimmunotherapy

Concurrent development of therapy−related acute myeloid leukemia (t−AML) and lymph node tuberculosis (LNTB) following comprehensive anti−tumor therapy for locally advanced lung squamous cell carcinoma (LSCC) is extremely rare in clinical practice. This is not a new biological concept but represents a rarely documented clinical scenario in the setting of neoadjuvant chemoimmunotherapy, surgery, and anti–PD−1 maintenance therapy. Herein, we systematically summarize the clinical features, pathogenesis and individualized therapeutic strategies of these two concurrent rare complications based on a single rare case and the latest relevant literature, to provide a reference for clinical diagnosis and treatment. A 54-year-old male patient was initially diagnosed with locally advanced LSCC. After four cycles of neoadjuvant therapy with carboplatin, albumin-bound paclitaxel and pembrolizumab, the tumor lesion regressed markedly. Thoracoscopic right upper lobectomy was then performed, followed by maintenance immunotherapy with single-agent pembrolizumab postoperatively. Four months after maintenance therapy, the patient developed abnormalities on routine blood work, low-grade fever, fatigue and superficial lymphadenopathy. t-AML was confirmed by bone marrow aspiration, immunophenotyping, gene mutation and cytogenetic examinations, accompanied by breast cancer susceptibility gene 2 (BRCA2), DNA (cytosine-5)-methyltransferase 3 alpha (DNMT3A), and isocitrate dehydrogenase 2 (IDH2) mutations, and positivity for lysine (K)-specific methyltransferase 2A partial tandem duplication (KMT2A-PTD). Meanwhile, LNTB was diagnosed by lymph node aspiration pathology combined with tuberculosis-specific assays. The patient was treated with an optimized quadruple anti-tuberculosis regimen (HZEM), and induction chemotherapy for AML with VA regimen (venetoclax plus azacitidine) plus revumenib, and supportive therapy. Subsequently, the patient achieved partial remission of leukemia, with no uncontrollable severe adverse events. In this case, LSCC was managed with neoadjuvant therapy, thoracoscopic right upper lobectomy and postoperative maintenance therapy with single agent pembrolizumab. The development of t−AML is primarily driven by cytotoxic DNA damage induced by chemotherapeutic agents, whereas the potential contribution of immune checkpoint inhibitors remains largely speculative. The potential contribution of immune checkpoint inhibitors via immune microenvironmental disturbance remains largely speculative and insufficiently documented by current clinical evidence. The impaired immune function caused by comprehensive anti-tumor therapy may further elevate the risk of LNTB. The overlapping clinical manifestations of the two concurrent diseases substantially increase diagnostic difficulty. Timely and thorough bone marrow examination, lymph node pathological biopsy and tuberculosis-specific screening are the keys to early and accurate diagnosis.